Molecular Characterization of Serine-, Alanine-, and Proline-Rich Proteins of
            <i>Trypanosoma cruzi</i>
            and Their Possible Role in Host Cell Infection

Baida, Renata Cristina Pardos; Santos, Marcia Rodrigues dos; Carmo, Mirian Silva do; Yoshida, Nobuko; Ferreira, Dalva E. C.; Ferreira, Alice Teixeira; El-Sayed, Najib M.; Andersson, Björn; Silveira, José Franco da

doi:10.1128/iai.74.3.1537-1546.2006

Cited by 35 publications

(40 citation statements)

References 42 publications

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“…A member of the cyclophilin family, CypA, is reported to be secreted by bloodstream form Trypanosoma congolense parasites (Pelle et al, 2002) but a function has not as yet been definitively ascribed to this protein. Also, Trypanosoma cruzi shed SAP proteins (Baida et al, 2006), although these are implicated in host cell invasion and so not relevant to the extracellular T. brucei. However, it is interesting to note that SAP proteins share some similarity with the T. cruzi MASP family, which, in turn, were weakly recognised in BLAST searches using ESAG9 sequences, but not other ESAGs.…”

Section: Discussionmentioning

confidence: 99%

Developmental regulation and extracellular release of a VSG expression-site-associated gene product from Trypanosoma brucei bloodstream forms

Barnwell

Deursen

Jeacock

et al. 2010

Journal of Cell Science

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SummaryTrypanosomes evade host immunity by exchanging variant surface glycoprotein (VSG) coats. VSG genes are transcribed from telomeric expression sites, which contain a diverse family of expression-site-associated genes (ESAGs). We have discovered that the mRNAs for one ESAG family, ESAG9, are strongly developmentally regulated, being enriched in stumpy forms, a life-cycle stage in the mammalian bloodstream that is important for the maintenance of chronic parasite infections and for tsetse transmission. ESAG9 gene sequences are highly diverse in the genome and encode proteins with weak similarity to the massively diverse MASP proteins in Trypanosoma cruzi. We demonstrate that ESAG9 proteins are modified by N-glycosylation and can be shed to the external milieu, this being dependent upon coexpression with at least one other family member. The expression profile and extracellular release of ESAG9 proteins represents a novel and unexpected aspect of the transmission biology of trypanosomes in their mammalian host. We suggest that these molecules might interact with the external environment, with possible implications for infection chronicity or parasite transmission.

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Section: Discussionmentioning

confidence: 99%

Developmental regulation and extracellular release of a VSG expression-site-associated gene product from Trypanosoma brucei bloodstream forms

Barnwell

Deursen

Jeacock

et al. 2010

Journal of Cell Science

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“…While some of those gene families are expressed throughout the parasite's life cycle, others have differential expression at a certain stage. Many of the genes expressed in trypomastigotes have been associated with recognition, adhesion and/or active cell invasion or escape of the immune response [22]–[33].…”

Section: Introductionmentioning

confidence: 99%

TcTASV-C, a Protein Family in Trypanosoma cruzi that Is Predominantly Trypomastigote-Stage Specific and Secreted to the Medium

et al. 2013

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Among the several multigene families codified by the genome of T. cruzi, the TcTASV family was the latest discovered. The TcTASV (Trypomastigote, Alanine, Serine, Valine) family is composed of ∼40 members, with conserved carboxi- and amino-termini but with a variable central core. According to the length and sequence of the central region the family is split into 3 subfamilies. The TcTASV family is conserved in the genomes of – at least – lineages TcI and TcVI and has no orthologues in other trypanosomatids. In the present work we focus on the study of the TcTASV-C subfamily, composed by 16 genes in the CL Brener strain. We determined that TcTASV-C is preferentially expressed in trypomastigotes, but it is not a major component of the parasite. Both immunoflourescence and flow cytometry experiments indicated that TcTASV-C has a clonal expression, i.e. it is not expressed by all the parasites of a certain population at the same time. We also determined that TcTASV-C is phosphorylated and glycosylated. TASV-C is attached to the parasite surface by a GPI anchor and is shed spontaneously into the medium. About 30% of sera from infected hosts reacted with TcTASV-C, confirming its exposition to the immune system. Its superficial localization and secretory nature suggest a possible role in host-parasite interactions.

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“…To invade mammalian cells, some surface glycoproteins present in metacyclic trypomastigotes, such as gp82, gp35/50 or gp30, known as a gp82 variant expressed in gp82-deficient isolates, trigger events that lead to intracellular Ca 2+ mobilization in both parasite and host cell (Burleigh and Andrews, 1998; Yoshida and Cortez, 2008). These parasites may also take advantage of secreted components, such as proteins from the SAP (serine-, alanine and proline-rich proteins) family; these proteins have a central domain (SAP-CD) responsible for invasion of mammalian cells by metacyclic forms (Baida et al, 2006; Zanforlin et al, 2013). Tissue culture-derived trypomastigotes (TCTs) have components, such as Tc-85, gp83, Tc-1, cruzipain, oligopeptidase B, and POP Tc80, that traverse the extracellular matrix and invade host cells (Burleigh and Andrews, 1998; Yoshida and Cortez, 2008).…”

Section: Invasion Mechanism Of Trypanosoma Cruzimentioning

confidence: 99%

“…The SAP-CD has regions SAP-NT (amino-terminal), SAP-CE (central), and SAP-CT (carboxy-terminal) (Baida et al, 2006). The interaction of SAP-CE fragment with host cells induce lysosome exocytosis by up-regulating calcium, probably acting synergistically with GP82 (Zanforlin et al, 2013).…”

Section: Modulation Mechanisms Of Extracellular Vesicles Cargomentioning

confidence: 99%

Mechanisms of Infectivity and Evasion Derived from Microvesicles Cargo Produced by Trypanosoma cruzi

Borges

Uehara

Dias

et al. 2016

Front. Cell. Infect. Microbiol.

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Cell invasion by the intracellular protozoans requires interaction of proteins from both the host and the parasite. Many parasites establish chronic infections, showing they have the potential to escape the immune system; for example, Trypanosoma cruzi is an intracellular parasite that causes Chagas disease. Parasite internalization into host cell requires secreted and surface molecules, such as microvesicles. The release of microvesicles and other vesicles, such as exosomes, by different eukaryotic organisms was first observed in the late twentieth century. The characterization and function of these vesicles have recently been the focus of several investigations. In this review, we discuss the release of microvesicles by T. cruzi. The molecular content of these vesicles is composed of several molecules that take place during parasite-host cell interaction and contribute to the parasite-driven mechanism of evasion from the host immune system. These new findings appear to have a profound impact on the comprehension of T. cruzi biology and highlight novel potential strategies for developing more efficient therapeutic approaches.

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Molecular Characterization of Serine-, Alanine-, and Proline-Rich Proteins of Trypanosoma cruzi and Their Possible Role in Host Cell Infection

Cited by 35 publications

References 42 publications

Developmental regulation and extracellular release of a VSG expression-site-associated gene product from Trypanosoma brucei bloodstream forms

Developmental regulation and extracellular release of a VSG expression-site-associated gene product from Trypanosoma brucei bloodstream forms

TcTASV-C, a Protein Family in Trypanosoma cruzi that Is Predominantly Trypomastigote-Stage Specific and Secreted to the Medium

Mechanisms of Infectivity and Evasion Derived from Microvesicles Cargo Produced by Trypanosoma cruzi

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